Dr. Robert Christensen and coworkers recently reported that neutropenia occurred in 49 percent of neonates delivered to women with pregnancy-induced-hypertension, that the neutropenia is the result of decreased neutrophil production, and that these neonates have a high rate of nosocomial infections (NEJM 32: 557, 1989). They now propose to employ studies of the production of hematopoietic growth factors and cultured hematopoietic progenitors to determine the mechanisms of the reduced neutrophil production. In other experiments, they found that high concentrations of erythropoietin (epo) down-modulate the production of neutrophils from progenitors, and that fetal progenitors are more sensitive to this effect than are those of adults (Blood 74: 817, 1989). They postulate that this mechanism underlies several different transient neonatal hyporegenerative neutropenias. They now propose to test this hypothesis using human and animal studies which evaluate the effect of high concentrations of epo on neutrophil storage, proliferative, and progenitor pools, and neutrophil production. Other experiments focus upon their observation that complete depletion of the neutrophil reserve is common in infected neonate and predicts a poor outcome (J Peds 98: 101, 1981). They now propose to define the molecular mechanisms used by normal adults to increase neutrophil production during bacterial infection, and to define the defect(s) that limit such increases in infected neonates. Finally, they recently described a unique kindred, containing seven individuals over three generations, affected with a neonatal hyporegenerative anemia (Am J Med Genetics, 1989). Using clonogenic marrow cell studies, they demonstrated that their defect involves impairment of the generation of normoblasts from erythroid progenitors. They postulate that study of the defective gene in this kindred will contribute to an understanding of the regulation of normal erythropoiesis, as well as identifying the defect in this family. They propose to begin such studies by determining the map-site location of the gene responsible for the anemia in this kindred, using DNA-linkage analysis.